ライフサイエンスコーパス: phosphatidyl inositol

1 n of a phosphate group to the 3'-position of phosphatidyl inositol.

2 human GPIT is EtN-P-2Manalpha1-4GlcN-(acyl)-phosphatidyl-inositol.

3 ERK (extracellular signal-regulated kinase), phosphatidyl inositol 3 (PI3)-kinase/Akt, and RalGEF/Ral

4 oss-linking of the FcepsilonRI activates the phosphatidyl inositol 3 kinase (PI3K) and mitogen-activa

5 epidermal growth factor receptor (ERBB1) or phosphatidyl inositol 3 kinase (PI3K) enhanced BBR3610 t

6 We found that inhibition of Ras, p38, phosphatidyl inositol 3 kinase (PI3K) or Akt signaling r

7 afenib cooperated with clinically relevant , phosphatidyl inositol 3 kinase (PI3K)-thymoma viral prot

8 ll as integrin-induced activation of Rho and phosphatidyl inositol 3 kinase, were compromised in Pyk2

9 This metabolic switch depends on the phosphatidyl inositol 3'-kinase/Akt pathway, is antagoni

10 teric site in complex with the head group of phosphatidyl inositol 3,4,5-trisphosphate and N-terminal

11 , RT-PCR using primers flanking the putative phosphatidyl inositol 3-kinase (PI3-K) binding site of E

12 3-methyl-adenine (3-MA), an inhibitor of phosphatidyl inositol 3-kinase (PI3-kinase) prevented in

13 on activation of the IGF-I receptor and the phosphatidyl inositol 3-kinase (PI3-kinase)-Akt pathway

14 ing, CD28 costimulation, and signals through phosphatidyl inositol 3-kinase (PI3K) and related metabo

15 wer cholesterol, possibly via recruitment of phosphatidyl inositol 3-kinase (PI3K) and the serine/thr

16 Phosphatidyl inositol 3-kinase (PI3K) is activated by IL

17 mitogen-activated protein kinase (MAPK) and phosphatidyl inositol 3-kinase (PI3K) signaling on the s

18 s glucose uptake through the insulin, IGF-1, phosphatidyl inositol 3-kinase (PI3K), and MAPK pathways

19 cation of a pharmacological inhibitor of the phosphatidyl inositol 3-kinase (PI3K).

20 le of nuclear factor kappa B (NF-kappaB) and phosphatidyl inositol 3-kinase (PI3K)/Akt signaling in t

21 was designed to investigate the role of the phosphatidyl inositol 3-kinase (PI3K)/AKT/p70(S6K) signa

22 ecombination, we assessed the effects of the phosphatidyl inositol 3-kinase inhibitor wortmannin on t

23 the pharmacological inhibitors wortmannin, a phosphatidyl inositol 3-kinase inhibitor, and leupeptin

24 the proteasome inhibitor, MG-132, or by the phosphatidyl inositol 3-kinase inhibitor, wortmannin.

25 In contrast, the activity of phosphatidyl inositol 3-kinase is not required for OGD p

26 nases (MAPKs) or protein kinase B/Akt of the phosphatidyl inositol 3-kinase pathway.

27 fects of anisomycin largely involved p38 and phosphatidyl inositol 3-kinase signaling mechanisms.

28 or OGD preconditioning because inhibition of phosphatidyl inositol 3-kinase with a chemical inhibitor

29 f NF-kappaB and found that they included the phosphatidyl inositol 3-kinase, protein kinase C, mitoge

30 ail of EGFR and attenuate phosphorylation of phosphatidyl inositol 3-kinase, which is recruited by EG

31 The phosphatidyl inositol 3-kinase-like kinases (PIKKs), ata

32 ne mutations that block its interaction with phosphatidyl inositol 3-kinase.

33 /11, protein kinase C, tyrosine kinases, and phosphatidyl inositol 3-kinase.

34 rotection was mediated, in part, through the phosphatidyl inositol 3-kinase/Akt and GSK-3beta pathway

35 laces the FRAP/mTOR kinase downstream of the phosphatidyl inositol 3-kinase/Akt-signaling pathway, wh

36 te, and a FYVE domain that selectively binds phosphatidyl inositol 3-phosphate.

37 ough nuclear factor kappa B (NF kappa B) and phosphatidyl-inositol 3 kinase (PI 3-kinase) since addit

38 rivatives or disruption of PDGFRalpha-driven phosphatidyl-inositol 3' kinase (PI3K) activity resulted

39 Nalpha treatment resulted in an mTOR- and/or phosphatidyl-inositol 3'(PI 3') kinase-dependent phospho

40 te myocytes is promoted by activation of the phosphatidyl-inositol 3'-kinase (PI3 kinase) pathway and

41 mma-32P]ATP results in the formation of [32P]phosphatidyl-inositol 3,4, 5-trisphosphate [PtdIns(3,4,5

42 It was also found that though inhibition of phosphatidyl-inositol 3-kinase (PI-3K) by LY294002 in al

43 tions in genes that encode components of the phosphatidyl-inositol 3-kinase (PI3-kinase) signaling pa

44 Extension formation requires phosphatidyl-inositol 3-kinase activity, whereas Rho kin

45 e plasma membrane via the Golgi complex in a phosphatidyl-inositol 3-kinase-dependent and actin-indep

46 g is dependent upon downstream activation of phosphatidyl-inositol 3-kinase/Akt, inactivation of the

47 In human lymphoblasts, NRG1-mediated phosphatidyl-inositol,3,4,5 triphosphate [PI(3,4,5)P3] s

48 als mediated by SRC family kinases SYK, CBL, phosphatidyl inositol-3 (PI-3) kinase, and Rac are direc

49 r tyrosine kinases, is a potent activator of phosphatidyl inositol-3 kinase (PI3K) and mammalian targ

50 ulated by growth factors and is sensitive to phosphatidyl inositol-3 kinase (PI3K) inhibitors.

51 The phosphatidyl inositol-3 kinase (PI3K) signaling pathway

52 ddition, other signaling pathways, including phosphatidyl inositol-3 kinase (PI3K), have the potentia

53 luding insulin receptor substrate-1 (IRS-1), phosphatidyl inositol-3 kinase (PI3K), Mammalian target

54 y inhibitors of ceramide-mediated apoptosis, phosphatidyl inositol-3 kinase activity, or tyrosine kin

55 cellular signal-regulated kinase kinase 1 or phosphatidyl inositol-3 kinase inhibition.

56 Incubation with a phosphatidyl inositol-3 kinase inhibitor or expression o

57 Our results show that inhibiting phosphatidyl inositol-3 kinase or blocking the interacti

58 hand, blockade of Ca2+, phospholipase C, or phosphatidyl inositol-3 kinase signaling pathways did no

59 Radiation-induced activation of the phosphatidyl inositol-3 kinase/Akt signal transduction p

60 he synthesis and biochemical validation of a phosphatidyl inositol-3 phosphate (PI3P) immunogen.

61 in monomers, and wortmannin, an inhibitor of phosphatidyl inositol-3-kinase (PI3-kinase), each disrup

62 ylates Chk1-Ser(280), the effect of Erbb2 on phosphatidyl inositol-3-kinase (PI3K)/Akt signaling duri

63 Inhibition of phosphatidyl inositol-3-kinase or mammalian target of ra

64 clic AMP; (ii) mediated by protein kinase C, phosphatidyl inositol-3-kinase, myosin light chain kinas

65 BKM-120 is a CNS-penetrant pan-class I phosphatidyl-inositol-3 kinase (PI3K) inhibitor in clini

66 The phosphatidyl-inositol-3 kinases (PI3K) pathway regulates

67 Activation of phosphatidyl-inositol-3'-OH-kinase (PI3K) and the result

68 inase (PI3K) and the resulting production of phosphatidyl-inositol-3,4,5-trisphosphate (PIP3) are ubi

69 nsequences of biochemical inhibition of KIT, phosphatidyl-inositol-3-kinase (PI3-K), PLCgamma, MAPK/E

70 ain-of-function alterations in MET, HER2, or Phosphatidyl-Inositol-3-Kinase (PI3K), catalytically ina

71 primary classes of effectors, namely, Rafs, phosphatidyl-inositol-3-kinases (PI3Ks) and Ral guanine

72 AP activity is stimulated by lipid messenger phosphatidyl inositol 4,5 bisphoshate (PI4,5P2) and is r

73 ossibly in combination with the reduction in phosphatidyl inositol 4,5 bisphosphate (PIP2).

74 f 0.59 muM and that this activation required phosphatidyl inositol 4,5-bisphosphate (PIP(2)).

75 gamma accumulation at cell-cell contacts and phosphatidyl inositol 4,5-bisphosphate production, which

76 Sac1 is a phosphatidyl inositol-4 phosphate (PI4P) lipid phosphata

77 ARF, an ATP-dependent step that requires the phosphatidyl-inositol-4 kinase Pik1, and third ATP-depen

78 nd sequesters acidic phospholipids including phosphatidyl-inositol-4,5-bisphosphate (PIP2) [7].

79 RF6 during neurite extension by coexpressing phosphatidyl-inositol-4-phosphate 5-Kinase alpha [PI(4)P

80 of Sec2p also binds to the Golgi-associated phosphatidyl-inositol-4-phosphate, which works in concer

81 bisphosphate (PtdInsP2) levels by activating phosphatidyl-inositol-4-phosphate-5-OH kinase (PtdIns-5-

82 ith its binding partners Ypt32p, Sec15p, and phosphatidyl-inositol-4-phosphate.

83 re that the N-WASP EVH1 domain does not bind phosphatidyl inositol-(4,5)-bisphosphate, as previously

84 s to the cell surface by means of a glycosyl-phosphatidyl-inositol anchor.

85 rminal domain with homology to GPI (glycosyl-phosphatidyl-inositol) anchor-containing proteins are se

86 CD16B is a glycosyl-phosphatidyl inositol-anchored molecule, whereas CD32A i

87 hosphatidic acid and phosphorylated forms of phosphatidyl inositol at least in part through the bindi

88 d implicates tubby domains as phosphorylated-phosphatidyl- inositol binding factors.

89 Changes in phosphatidyl inositol bisphosphate (PIP2) concentration

90 that mice who are deficient in the glycosyl-phosphatidyl inositol (GPI) -linked protein GFRalpha1 (G

91 essing site close to the C-terminal glycosyl phosphatidyl inositol (GPI) membrane anchor site, which

92 and the sequence predicted it was a glycosyl phosphatidyl inositol (GPI)-anchored protein that had a

93 action was further examined using a glycosyl phosphatidyl inositol (GPI)-linked form of CD45Null (lac

94 ision abnormally delayed (dally), a glycosyl-phosphatidyl inositol (GPI)-linked glypican, as a hepara

95 en used to manipulate and concentrate glycan-phosphatidyl inositol (GPI)-tethered proteins in planar

96 lipoprotein lipase (LpL) with a glycosylated phosphatidyl-inositol (GPI) anchor in cardiomyocytes hav

97 R) has been identified as an axonal glycosyl-phosphatidyl-inositol (GPI)-anchored protein, whereas th

98 Glutamate stimulates phosphatidyl inositol hydrolysis and mobilizes intracell

99 ctasia mutated ( ATM ) gene, a member of the phosphatidyl inositol kinase-like (PIKL) family of prote

100 Consecutive phosphatidyl inositol kinase-like kinase (PIKK)-dependen

101 expressing neurons also express the glycosyl-phosphatidyl inositol-linked (GPI-linked) GDNF binding c

102 tastasis-associated protein CD24, a glycosyl phosphatidyl inositol-linked surface protein, as a downs

103 Phosphatidyl-inositol mannosides (PIM) are glycolipids u

104 ocalised production of PI(4,5)P(2) by type 1 phosphatidyl inositol phosphate kinase type 1gamma (PIPK

105 d composition, including bilayers containing phosphatidyl inositol phosphates.

106 transduction pathway requires Akt binding to phosphatidyl-inositol phosphates (PIP) on the cell membr

107 pheral membrane proteins which interact with phosphatidyl-inositol phosphates (PIPs) in cell membrane

108 eads to an increase in phospholipids such as phosphatidyl inositols, phosphatidyl serines, phosphatid

109 Inhibition of the phosphatidyl inositol (PI) 3-kinase intermediate in IGF-

110 studied biochemical response: stimulation of phosphatidyl inositol (PI) hydrolysis].

111 In vitro phosphatidyl inositol (PI) kinase assay demonstrated tha

112 LRH-1-which reveal that these receptors bind phosphatidyl inositol second messengers and that ligand

113 osphorylation of several proteins, including phosphatidyl inositol-specific phospholipase C-gammal.

114 ants and that prevention of this accelerated phosphatidyl-inositol turnover in turn negates suppressi

115 lipid classes, i.e. phosphatidyl-choline and phosphatidyl-inositol, were differentially affected by t